Effects of Starvation on Antioxidant-Related Signaling Molecules, Oxidative Stress, and Autophagy in Juvenile Chinese Perch Skeletal Muscle.

Abstract

The autophagic lysosomal protein degradation pathway is an evolutionarily conserved pathway, which utilizes lysosomes to degrade and to circulate cell components. Autophagy has been observed in many different types of cells, but its role in skeletal muscle protein degradation has not been thoroughly studied, especially in aquatic species. This study assessed the expression of antioxidant-related signaling genes and the effects of starvation on antioxidant capacity, reactive oxygen species (ROS) content, autophagy-related gene, and autophagosome formation in the skeletal muscle of juvenile Chinese perch after short-term starvation. The results indicated that after starvation for 2days, the expression of antioxidant-related signaling genes, such as Nrf2 and S6K, was upregulated, while Keap1 was downregulated in the muscle of juvenile Chinese perch. The amounts of antioxidant enzymes ROS, MDA, AHRFR, and ASA and the activities of SOD, CAT, GPx, and GST were increased, and the mRNA levels of GPx, GSTA, GST4A, GSTT1, MnSOD, ZnSOD, and CAT were upregulated. Meanwhile, there was no significant change in the level of LC3-II protein. When starvation was prolonged to 5days, Nrf2 and S6K1 continued to increase and mTOR and Keap1 significantly decreased; ROS and ASA content continued to be significantly increased, but the MDA and AHRFR content and the SOD, CAT GR, and GPx activities all decreased. The expression of MnSOD, ZnSOD, and GR decreased significantly, and GST4A, GSTT1, and CAT tended to decrease to levels consistent with normal feeding. The expression of all autophagy-related genes except Ulk1 significantly increased, the formation of autophagosomes and autolysosomes was enhanced in muscle, and LC3 protein levels in muscle increased significantly. Our data suggested that the autophagy that occurs in the skeletal muscle tissue of Chinese perch due to dietary deprivation is involved in a series of molecular and physiological responses, including changes in antioxidant signaling molecules, in antioxidant capacity and in autophagy and autophagy-related gene expression.